Bex2 regulates cell proliferation and apoptosis in malignant glioma cells via the c-Jun NH2-terminal kinase pathway

• Published in: Biochemical and biophysical research communications 2012-10, Vol.427 (3), p.574-580
• Main Authors: Zhou, Xiuping, Meng, Qingming, Xu, Xuebin, Zhi, Tongle, Shi, Qiong, Wang, Yong, Yu, Rutong
• Format: Article
• Language: English
• Subjects: 60 APPLIED LIFE SCIENCES; Anthracenes - pharmacology; APOPTOSIS; Bex2; BRAIN; Cell Line, Tumor; CELL PROLIFERATION; Down-Regulation; GENES; Glioma; Glioma - metabolism; Glioma - pathology; GLIOMAS; Humans; JNK; JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors; JNK Mitogen-Activated Protein Kinases - metabolism; Nerve Tissue Proteins - genetics; Nerve Tissue Proteins - metabolism; Proliferation; Protein Kinase Inhibitors - pharmacology; Signal Transduction
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2012.09.100

► The expression levels of Bex2 markedly increased in glioma tissues. ► Bex2 over-expression promoted cell proliferation, while its down-regulation inhibited cell growth. ► Bex2 down-regulation promoted cell apoptosis via JNK/c-Jun signaling pathway. The function of Bex2, a member of the Brain Expressed X-linked gene family, in glioma is controversial and its mechanism is largely unknown. We report here that Bex2 regulates cell proliferation and apoptosis in malignant glioma cells via the c-Jun NH2-terminal kinase (JNK) pathway. The expression level of Bex2 is markedly increased in glioma tissues. We observed that Bex2 over-expression promotes cell proliferation, while down-regulation of Bex2 inhibits cell growth. Furthermore, Bex2 down-regulation promotes cell apoptosis and activates the JNK pathway; these effects were abolished by administration of the JNK specific inhibitor, SP600125. Thus, Bex2 may be an important player during the development of glioma.